In this paper using human peripheral lymphocytes, we first show that TQ can cause oxidative DNA breakage in cells through mobilization of endogenous copper ions.
Together, these observations show that Aptx−/− MEFs exhibit no detectable defect in global repair of oxidative DNA breakage yet they possess an accelerated senescence and reduced transcription recovery following acute doses of oxidative stress.
Moreover, researchers are finding evidence that ( {text{Fe}}_{3} {text{O}}_{4} ) NPs exposure can produce mutagenic effects including: chromosomal aberrations, DNA strand breakage, oxidative DNA damage and mutations (Koedrith et al. 2014).
Using human peripheral lymphocytes and comet assay, we first show that TQ is able to cause oxidative cellular DNA breakage.
In DNA damage, H2O2 generates OH· as shown in Eq. 4, which are responsible for DNA breakage through oxidative reaction (Eq. 5) [85] 85].
Thus, the modified DNA is resistant to growth inhibition and oxidative double-stranded DNA breakage caused by H2O2 [ 9].
Besides direct glycation damage to protein, MG reacting with lysine may contribute to oxidative DNA damage, strand breakage and cell apoptosis [ 5, 6].
The results given in Figure 5 along with the above results of comet assay indicate that both DNA breakage and oxidative stress in cells is inhibited by Cu(I) chelation and scavenging of reactive oxygen.
Oxidative stress-dependent DNA breakage and repair and activation of signaling pathways including poly-ADP-ribose polymerase (PARP), AP-1, NF- κB, p38, and Akt were reported in human mesothelial cells exposed to SWCNT [ 93].
NO, especially in high concentrations, causes the deamination of deoxynucleotides, DNA strand breakage and oxidative damage from peroxynitrite, and DNA modification by metabolically activated N-nitrosamines, all of which can lead to somatic mutations.
